Human parathyroid hormone dilates both pig coronary and human inferior epigastric arteries by a cyclic AMP-dependent pathway.

Human parathyroid hormone (hPTH (1-38)) induced concentration-dependent relaxations in prostaglandin F2 alpha-preconstricted pig coronary arteries in vitro. Removal of endothelial cells or pretreatment with nitro-L-arginine, a specific inhibitor of the endothelium-derived relaxing factor (EDRF) synthesis, impaired, although to a small extent, hPTH-induced relaxations. Human PTH-, but not bradykinin- or nitroglycerin-induced relaxations were potentiated in the presence of the cyclic AMP phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX). Human PTH also relaxed preconstricted human inferior epigastric arteries in vitro. In accordance to pig coronary arteries, this relaxation was potentiated in the presence of IBMX. However, the human internal thoracic (mammary) artery did not respond to hPTH (1-100 nM). Thus, acute vasodilatory effects of hPTH may not be present in all human arteries. The physiological significance of this phenomenon is not known. This relaxation, at least in pig arteries, is mediated to a small extent by the release of EDRF. In addition, this relaxation appears to be mainly mediated in both pig and human arteries by a smooth muscle cyclic AMP pathway.